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Identification of the gene expression in IPF lung fibroblasts after demethylation

ABSTRACT: Idiopathic pulmonary fibrosis (IPF) is a progressive lung disease. Although the pathogenesis is poorly understood, evidence suggests that genetic and epigenetic alterations, such as DNA methylation, may play a key role. We used microarrays to see the gene expression in IPF fibroblasts after demethylation agent 5'-azacytidine treatment. Human IPF lung fibroblasts were cultured and then treated with 5'-azacytidine 5uM 24 hours. RNA were extracted and hybridized on Affymetrix microarrays.

ORGANISM(S): Homo sapiens

SUBMITTER: ting Xie

PROVIDER: E-GEOD-69764 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Methylation-mediated BMPER expression in fibroblast activation in vitro and lung fibrosis in mice in vivo.

Huan Caijuan C Yang Ting T Liang Jiurong J Xie Ting T Cheng Luis L Liu Ningshan N Kurkciyan Adrianne A Monterrosa Mena Jessica J Wang Chen C Dai Huaping H Noble Paul W PW Jiang Dianhua D

Scientific reports 20151007

Idiopathic pulmonary fibrosis (IPF) is a progressive lung disease. Although the pathogenesis is poorly understood, evidence suggests that genetic and epigenetic alterations, such as DNA methylation, may play a key role. Bone morphogenetic proteins (BMPs) are members of the transforming growth factor-β (TGF-β) superfamily and are important regulators in IPF. Here we identified BMP endothelial cell precursor-derived regulator (BMPER) as a key regulator of fibroblast activation. BMPER is a secreted ...[more]

PMID: 26442443

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Spatial transcriptomics (Visium, 10x Genomics) data for human Idiopathic Pulmonary Fibrosis (IPF) and control lung tissue

Project description:Visium (10x Genomics) spatially resolved transcriptomics data generated from normal and Idiopathic Pulmonary Fibrosis (IPF) lung parenchyma tissues collected from human donors. The fresh-frozen tissues that were analyzed were from four healthy control (HC) subjects and from four IPF patients. For each IPF patient, three different tissues were selected representing areas of mild (“B1”), moderate (“B2\") or severe (“B3”) fibrosis within the same donor, as determined by histological inspection of Hematoxylin and Eosin (H&E)-stained samples. Data from a total of 25 tissue sections, from 16 unique lung tissue blocks. The lung tissues were collected post-mortem (HC donors) or during lung transplant/resection (IPF patients) after obtaining informed consent. The study protocols were approved by the local human research ethics committee (HC: Lund, permit number Dnr 2016/317; IPF: Gothenburg, permit number 1026-15) and the samples are anonymized and cannot/should not be traced back to individual donors.

2024-05-28 | E-MTAB-14121 | biostudies-arrayexpress

Identification of the gene expression in IPF lung fibroblasts after demethylation

Project description:Idiopathic pulmonary fibrosis (IPF) is a progressive lung disease. Although the pathogenesis is poorly understood, evidence suggests that genetic and epigenetic alterations, such as DNA methylation, may play a key role. We used microarrays to see the gene expression in IPF fibroblasts after demethylation agent 5'-azacytidine treatment.

2016-02-16 | GSE69764 | GEO

Forkhead Box F1 (FOXF1) represses fibroblast functions relevant to fibrogenesis

Project description:Aberrant expression of master phenotype regulators by lung fibroblasts may play a central role in idiopathic pulmonary fibrosis (IPF). Interrogating IPF fibroblast transcriptome datasets, we identified Forkhead Box F1 (FOXF1), a DNA-binding protein required for lung development, as a candidate actor in IPF. Thus, we determined FOXF1 expression levels in fibroblasts cultured from normal or IPF lungs in vitro, and explored FOXF1 functions in these cells using transient and stable loss-of-function and gain-of-function models. FOXF1 mRNA and protein were expressed at higher levels in IPF compared with controls. In normal lung fibroblasts, FOXF1 repressed key fibroblast functions such as proliferation, survival, and expression of collagen-1 (COL1) and actin related protein 2/3 complex, subunit 2 (ARPC2). ARPC2 knockdown mimicked FOXF1 overexpression with regard to proliferation and COL1 expression. FOXF1 expression was induced by the antifibrotic mediator prostaglandin E2 (PGE2). Ex vivo, FOXF1 knockdown conferred CCL-210 lung fibroblasts the ability to implant and survive in uninjured mouse lungs. In IPF lung fibroblasts, FOXF1 regulated COL1 but not ARPC2 expression. In conclusion, FOXF1 functions and regulation were consistent with an antifibrotic role in lung fibroblasts. Higher FOXF1 levels in IPF fibroblasts may thus participate in a compensatory response to fibrogenesis. Lung fibroblasts derived from 4 different IPF patients (P313, P355, P375 and P426) were transiently transfected with pcfoxf1 or control pcDNA3.1-constructs. Total RNAs were extracted 24 h after transfection and hybridized on microarrays. One color experiment with 2 experimental conditions: pcfoxf1 and pcDNA3.1

2014-10-01 | E-GEOD-52612 | biostudies-arrayexpress

PRM detection of NEDD4-2 in human IPF and control tissue

Project description:Idiopathic pulmonary fibrosis (IPF) is a chronic progressive interstitial lung disease characterized by patchy scarring of the distal lung with limited therapeutic options and poor prognosis. Here, we show that conditional deletion of the ubiquitin ligase Nedd4-2 in lung epithelial cells in adult mice produces chronic lung disease that shares key features with IPF including progressive fibrosis and bronchiolization with increased expression of Muc5b in peripheral airways, honeycombing and characteristic alterations in the lung proteome.

2020-03-20 | PXD011129 | Pride

Gene expression signatures for Normal-looking, fibrotic foci and hyperplastic (adjacent to fibrotic foci) area in IPF lungs

Project description:To further understand the pathologic microenvironment in IPF, we have employed whole genome microarray expression profiling as a discovery platform to identify genes with the potential to distinguish normal and IPF lung in normal-looking, fibrotic foci and hyperplastic areas of IPF lung. Four IPF lungs were dissected into normal-looking, fibrotic foci and hyperplastic areas by Laser-Capture-Microdissection. Gene expression analysis showed that 638 significantly different genes were identified that clearly distinguished the different IPF microenvironments . Among them, MMP19 was revealed as one of the most significantly up-regulated genes that distinguished normal looking epithelial cells (N) to hyperplastic epithelial cells, MMP19 up-regulation in IPF lungs was verified by immunohistochemical (IHC), qRT-PCR and Western-blot. IPF lungs are heterogeneity complex, which comprise normal looking area, fibrotic foci and hyperplastic area. In this study we separated the normal, fibrotic foci and hyperplastic area by LCM and employed Agilent whole genome gene expression microarray profiling to identify genes with the potential to distinguish the unique microenironment of IPF

2013-01-11 | E-GEOD-35309 | biostudies-arrayexpress

Bulk RNA-seq on SEMA7A high and negative Idiopathic pulmonary fibrosis (IPF) lung fibroblasts

Project description:To check the gene signatures of SEMA7A high and SEMA7Anegative IPF lung fibroblasts and the similarity of SEMA7A high fibroblasts and invasive fibroblasts, SEMA7A negative fibroblasts and noninvasive fibroblasts, we sorted the SEMA7A high and negative IPF lung fibroblasts by flow cytometry and performed total RNA-seq.

2019-12-31 | GSE137025 | GEO

Comparison of Azithromycin treated and non-treated human lung fibroblasts

Project description:Azithromycin has been shown to have anti-fibrotic effects on idiopathic lung fibroblasts (IPF). We thus wanted to investigate involved genes and pathways by microarray analysis. We treated normal human lung fibroblasts with Azithromycin (50uM) for 24h and compared them to non-treated samples.

2019-11-07 | E-MTAB-8488 | biostudies-arrayexpress

The profile of miRNAs in lung fibroblast-derived extracellular vesicles from idiopathic pulmonary fibrosis (IPF) patients or non-IPF individuals.

Project description:Accelerated senescence in lung epithelial cells is known to play a key role in the pathogenesis of idiopathic pulmonary fibrosis (IPF). However, the exact mechanisms underlying the IPF-related epithelial cell phenotype have yet to be elucidated. Increasing evidence supports the concept that extracellular vesicles (EVs), including exosomes and microvesicles, mediate intercellular communication that contributes to diverse aspects of physiology and pathogenesis. Here, we demonstrate that lung fibroblasts (LFs) from IPF patients accelerate epithelial cell senescence via EV-mediated transfer of LF-derived pathogenic cargo to lung epithelial cells. Mechanistically, IPF LF-derived EVs increase mitochondrial reactive oxygen species (mtROS) and associated mitochondrial damage in lung epithelial cells, leading to mtROS-mediated activation of the DNA damage response and subsequent epithelial cell senescence. We show that IPF LF-derived EVs contain elevated levels of miR-23b-3p and miR-494-3p that are responsible for suppressing SIRT3, resulting in the EV-induced phenotypic changes of lung epithelial cells. Furthermore, we observe that miR-23b-3p and miR-494-3p expression increases in lung epithelial cells from IPF patients’ lungs. Finally, the levels of miR-23b-3p and 494-3p found in IPF LF-derived EVs correlate positively with IPF disease severity. These findings reveal that the accelerated epithelial cell mitochondrial damage and senescence observed during IPF pathogenesis are caused by a novel mechanism in which SIRT3 is suppressed by miR-containing EVs derived from IPF fibroblasts.

2020-08-04 | GSE124665 | GEO

Expression data from lung tissues of IPF patients and Normal Control

Project description:Idiopathic pulmonary fibrosis (IPF) is a progressive lethal interstitial lung disease of unkown etiology with limited effective therapies. The pathogenic mechanisms of IPF remain unkown. Emerging evidences indicate that abnormal behaviors of fibroblasts in IPF are associated with a variety of genetic alterations and aberrant reactivation of developmental signaling pathways. We compared gene expression profiles in fibrotic lung tissues from IPF patients and normal lung tissues from patients with primary spontaneous pneumothorax using cDNA microarray to examine the mechnisms involved in the pathogenesis of IPF.

2015-08-15 | GSE72073 | GEO

Differences between fibroblasts derived from normal and IPF lungs

Project description:Objective: To evaluate the characteristics of IPF lungs in fibroblasts, we performed RNA-Sequencing of fibroblasts derived from normal and IPF lungs Method:　NHLF（Normal human lung fibroblast）　and DHLF-IPF (DIPF; Diseased human lung fibroblasts derived from idiopathic pulmonary fibrosis)　were purchased from Lonza (Walkersville, MD, USA) .Total RNA was extracted from fibroblasts (NHLF and DIPF) using an RNeasy® Mini Kit (#74106; Qiagen, Valencia, CA, USA). Preparation of a next-generation sequencing library was performed using a SMARTer® Stranded Total RNA Sample Prep Kit–Pico Input Mammalian (TaKaRa, Shiga, Japan). Sequencing was performed on an Illumina HiSeq 2500 platform in 75-base single-end mode with Illumina Casava 1.8.2 software for base calling. Sequenced reads were mapped to the human reference genome sequence (hg19) using TopHat v.2.0.13 software, in combination with Bowtie 2 v.2.2.3 and SAMtools v.0.1.19. Result: Of the 26,257 genes analyzed, for NHLF and DHLF-IPF (DIPF), FPKM was required to be greater than or equal to 0.3. Under these conditions, 764 genes were up regulated inDHLF-IPF (DIPF) and 691 genes were down regulated.

2021-10-06 | GSE185259 | GEO

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